Delayed overt hemolytic transfusion reaction due to anti-U antibody

A patient is described who developed a delayed hemolytic transfusion reaction, 11 days posttransfusion, caused by anti-U. This case illustrates the difficulty that can occur in distinguishing a delayed transfusion reaction from autoimmune hemolytic disease when the antibody involved is directed against a high incidence blood group antigen.     

Fetal hemolytic anemia and intrauterine death caused by anti-M immunization

BACKGROUND: Antibodies with anti-M specificity are detected in 10 percent of pregnant women with a positive antibody screen, but anti-M is only rarely associated with hemolytic anemia in the fetus. STUDY DESIGN AND METHODS: This study reports on three pregnancies in one family that all resulted in severe fetal anemia. The first fetus died in utero with hydrops fetalis during the 20th gestational week and the second child was delivered after 28 weeks of gestation with hydrops fetalis and a hemoglobin level of 16 g per L whereas the third affected child was treated with intrauterine red cell (RBC) transfusions before delivery at 28 weeks of gestation. RESULTS: The direct antiglobulin test was negative but anti-M in a low titer was detected through the three pregnancies, and its clinical relevance, which initially was uncertain, was confirmed by pronounced in vivo hemolysis in maternal blood of chromate ((51)Cr)-labeled M+ RBCs and normal survival of (51)Cr labeled M- RBCs. CONCLUSION: It is concluded that anti-M immunization in a few cases may cause severe fetal hemolytic anemia and intrauterine death. It remains to be elucidated why a normally clinically insignificant antibody is this aggressive in a small proportion of cases. Because the condition is treatable, anti-M must be considered as a possible cause of fetal anemia and intrauterine death.     

Carboxyhemoglobin elevation due to hemolytic anemia

A critically ill man with drug-induced hemolytic anemia and hepatic failure was hospitalized at a private academic medical center in Seattle, Washington. Intravascular hemolysis with associated endogenous carbon monoxide (CO) production resulted in elevation of the patient's carboxyhemoglobin (COHb) level to as high as 9.7%. Serial measurements of the patient's COHb level were obtained and compared with other conventional measures of hemolytic activity. With the availability of new non-invasive measurement technology to detect COHb elevations, emergency clinicians are likely to see COHb elevation as a manifestation of hemolytic anemia.     

Three episodes of delayed hemolytic transfusion reactions due to multiple red cell antibodies, anti-Di, anti-Jk and anti-E

There is no report in which three episodes of delayed hemolytic transfusion reaction (DHTR) occurred from multiple antibodies to red cells (RBCs) in the course of treatment of a patient. This paper describes episodes of anemia and hyperbilirubinemia in concert with the development of three alloantibodies in a multiple transfused patient. The patient was a 71-year-old male suffering from valvular heart disease and hemophilia B with a history of transfusions. Although he received compatible RBCs from 14 donors as judged by a crossmatch test using the albumin-antiglobulin method, three episodes of DHTR occurred after surgery. The first hemolytic episode on day 7 after surgery was due to anti-Di(a) because of clinical and laboratory evidence which included jaundice, sudden increases in total bilirubin (T-Bil) and lactate dehydrogenase (LD) levels, and a decrease (2.2 g/dl) in hemoglobin (Hb) level. The second hemolytic episode on day 16 resulted from newly producted anti-Jk(b). The patient experienced fever, fatigue, nausea and anorexia, and laboratory data showed a second increase in T-Bil, a second decrease (3 g/dl) in Hb, and moderate elevations of blood urea nitrogen (BUN) and creatinine (CRE) levels. The third hemolytic episode on day 39 was due to anti-E. The patient complained of fever and fatigue and had a third unexplained drop (1.5 g/dl) in Hb despite no bleeding. This is the first reported case in which three episodes of DHTR occurred from different red cell antibodies.     

Fatal immune hemolytic anemia due to cefotetan

In the first death associated with immune hemolytic anemia due to cefotetan, the patient developed hemolytic anemia and renal failure, dying 12 days after the beginning of 1 week's cefotetan therapy. The patient's serum contained strong antibodies reacting with cefotetan-treated red cells (RBCs) and with uncoated RBCs in the presence of cefotetan; a much weaker, drug-independent antibody was also detected. Three-days before the patient's death, the antibody reacting with cefotetan-coated RBCs rose to a titer of 262,144; the titer of the antibody to uncoated RBCs, in the presence of cefotetan, rose to 2048; the titer of the drug-independent antibody remained at 4.     

A delayed hemolytic transfusion reaction due to anti-Cob

A delayed hemolytic transfusion reaction precipitated by anti-Cob is described in a multiple transfused primigravida woman with sickle-cell disease. Sixteen days after the prophylactic transfusion of the first of 4 units of red cells, she experienced a fall in hemoglobin concentration accompanied by a newly positive antibody screen and direct antiglobulin test. Anti-Cob was identified both in the patient's serum and in an eluate prepared from her red cells.     

Donath-Landsteiner hemolytic anemia due to an anti-Pr-like biphasic hemolysin

Anemia, hyperbilirubinemia, and reticulocytosis subsequent to viral infection were present in a 32-year-old woman. The direct antiglobulin test was negative, and no unexpected antibodies were detected in pretransfusion tests. Rosettes of red cells (RBCs) around neutrophils were observed in peripheral blood smears, and a Donath-Landsteiner (D-L) test was positive. However, the patient did not show the classic features of paroxysmal cold hemoglobinuria (PCH). There was no hemoglobinuria, and in vivo hemolysis was not precipitated by cold. The D-L antibody was IgG, but classic anti-P specificity was not apparent. Rather, protease- or neuraminidase-treated RBCs, as well as certain sialic acid deficient RBCs of uncommon MN phenotypes, were not hemolyzed in D-L tests. Further, D-L antibody activity could be inhibited by MN sialoglycoprotein. These data support a diagnosis of chronic D-L hemolytic anemia, caused by an anti-Pr-like biphasic hemolysin.     

Delayed hemolytic transfusion reactions in sickle cell anemia

Delayed hemolytic transfusion reaction (DHTR) developed in three patients with sickle cell anemia seen over an 18-month period at Cook Country Hospital. The DHTR was associated with severe pain crisis, with spherocytic hemolytic anemia, a positive direct antiglobulin test result, previously undetected erythrocyte alloantibodies, and disappearance of Hb A on cellulose acetate electrophoresis. Delayed hemolytic transfusion reactions may be more common than is generally recognized and should be considered when a patient has a sickle cell pain crisis shortly after receiving a transfusion.     

Fatal delayed hemolytic transfusion reaction due to anti-c + E

A 72-year-old man with a peptic ulcer received seven units of apparently compatible red blood cells. Six days after the last unit, he had a hemolytic transfusion reaction manifested by high fever, marked fall in hematocrit, hemoglobinemia, hemoglobinuria, severe bilirubinemia and oliguria. He went on to become uremic, hyperkalemic, anuric and died five days later. Serologic studies showed that the donor and recipient bloods were completely compatible prior to the transfusions and that unexpected antibodies were not detected. The anamnestic response from donor antigens was precipitous even after a latent period of six days.     

Delayed hemolytic transfusion reaction caused by anti-P1 antibody

A 67-year-old white woman received transfusions of a total of 87 units of whole blood and red blood cells during and within 48 hours following a pneumonectomy. Although she had previously received blood transfusions, unexpected antibodies were not detectable by routine screening. On the second postoperative day, she developed fever, hemoglobinemia, hemoglobinuria, and oliguria. However, the direct antiglobulin test and the antibody screen were negative. On the eighth postoperative day, an IgM anti-P1 antibody was detected for the first time. This anti-P1 antibody increased in thermal amplitude from 22 to 37 C, but remained IgM. The circulating transfused P1-positive cells decreased progressively without evidence of bleeding. Testing of the patient's preoperative blood at 15 C found her serum to be weakly reactive with P1 cells, while her own cells were P2. Thus, an anamnestic response to the P1 antigen is the most likely cause of her delayed hemolytic transfusion reaction.     

The first case of drug-induced immune hemolytic anemia due to hydrocortisone

BACKGROUND: Drug‐induced immune hemolytic anemia (DIIHA) is a well‐known complication of drug treatment. Sensitization can occur, due to interaction of the drug and/or its metabolites with cells of the immune system, after the first drug administration, while the hemolytic crisis generally occurs after repeated administration of a drug. This event occurred in the case described here of acute hemolysis due to the administration of corticosteroids. STUDY DESIGN AND METHODS: To define the etiopathogenesis of the hemolytic crisis, immunohematologic screening and specific tests were performed to identify antibodies against a possible drug–red cell (RBC) complex and circulating drug–anti‐drug antibody immune complexes. Six drugs administered to the patient were tested and results were confirmed by test repetition using other types of corticosteroids. RESULTS: Indirect antiglobulin test performed with the patient's serum sample on 22 RBC samples from commercial panels was strongly positive, while it was negative on RBCs from ABO‐compatible donors. The same test repeated on commercial RBCs after washing was negative. Specific tests were negative for five of the six tested drugs, while RBCs incubated with hydrocortisone strongly reacted with the patient's serum. The same tests performed using other types of corticosteroids confirmed a reaction with the same positivity score on all tested molecules. CONCLUSION: The positive reaction observed each time the patient's serum sample was incubated with RBCs in the presence of corticosteroids suggested that the triggering cause of hemolysis was an immune‐mediated mechanism and the drug responsible for DIIHA was hydrocortisone.     

Delayed presentation of prosthetic joint infection due to Listeria monocytogenes

Infection with Listeria monocytogenes is rare and has been described in prosthetic valves, stent grafts and prosthetic joints. The route of infection appears to be haematogenous. The choice between conservative treatment with antibiotics or surgical treatment with debridement and revision of the components remains controversial. The best antibiotic treatment is not known with ampicillin being the first choice in most cases. Prosthetic infections with Listeria monocytogenes usually occur in patients with malignancy, diabetes mellitus, chronic renal disease, liver disease, elderly patients and patients receiving immunosuppressive therapy. The hip is the commonest prosthetic joint affected followed by the knee. We report the seventh case of Listeria monocytogenes infection in a non-immunocompromised patient involving a prosthetic joint.